CASE 3 HYPOTHESIS 2

INFLAMMMATION

Pathophysiology and source of clinical signs

Arthritis - preliminary localization of lameness to 
fetlock area by physical 
exam/observation, no instability noted

a. Damage to chondrocytes or cartilage matrix (see 
etiologies)
b. Increased anabolic/catabolic activity of 
chondrocytes due to damage
c. Increased production of metalloproteinases
d. Release of inflammatory mediators 
(cytokines/prostaglandins)from chondrocyte 
catabolism
e. Catabolism exceeds anabolism
f. Cartilage degradation
- decreased tensile strength of collagen
- proteoglycans swell
- abnormal cartilage structure now unable to 
withstand normal forces within 
joint
- perpetuation of damage
g. subchondral bone eventually thickens in response 
to increased abnormal 
stress; 
bone remodelling/osteophytes
h. Inflammatory mediators cause hypertrophy and 
hyperplasia of synovial lining 
layer and fibroplasia of fibrous capsule Ü joint 
capsule thickening
i. Increased permeability of synovial vasculature 
due to inflammatory mediators 
facilitates swelling
j. Pain from swelling Ü stretching of the richly 
innervated joint capsule and 
biochemical stimulation of nociceptors by 
inflammatory mediators creates the 
clinical lameness and foalÍs reluctance to bear 
weight
k. Fluid accumulation and inflammatory exudate in 
the joint creates an 
excessively viscous joint fluid that is slow to 
flow back into place when 
displaced by digital pressure (pitting edema)


Possible etiologies for foalÕs arthritis

1. Trauma Ü sprain, luxation, fracture, joint 
capsule, or tendon damage that 
leads to damage to chondrocytes or cartilage matrix 
and consequently begins 
chain of inflammatory events in the joint.  
Possible injury from being stepped 
on by the mare as suggested by the client would 
support this etiology.

2. Septic arthritis - bacterial seeding and 
colonization of the synovial 
lining/fluid; inflammatory response to bacteria 
sets up for enzymatic 
degradation and damage to chondrocytes and/or 
cartilage matrix

a. penetrating trauma which innoculates joint with 
bacteria - horses have 
minimal soft tissue covering over joints; would 
also explain limited involvement 
of the fetlock in the arthritic process and 
possibly the lack of systemic 
response

b. hematogenous infection of joint  - common in 
neonates due to umbilical portal 
of entry for bacteria; failure of passive transfer 
is an important predisposing 
factor; would often expect multiple joint 
involvement and possible systemic 
illness, also two weeks is older than one would 
expect with this condition

c. extension of osteomyelitis - adjacent infected 
epiphysis or metaphysis could 
seed joint space